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Submitted on October 7, 2005
Accepted on February 15, 2006
University of Adelaide Department of Medicine, Royal Adelaide Hospital, Adelaide, South Australia, Australia, Diabeteszentrum, Bad Lauterberg, Germany
* To whom correspondence should be addressed. E-mail: christine.feinle{at}adelaide.edu.au.
Context: The inhibitory action of glucagon-like peptide-1 (GLP-1) on gastric emptying (GE) is likely to be important in mediating its effects on postprandial glycemia, appetite and gastrointestinal symptoms.
Objective: To evaluate the effects of "low" and "high" doses of i.v. GLP-1 on GE, intragastric meal distribution, glycemia, insulinemia and appetite.
Design: 10 healthy males were studied on 3 days. GE of a solid (ground beef)/liquid (glucose) meal, blood glucose, plasma insulin, glucagon and GIP, appetite perceptions and gastrointestinal symptoms were evaluated during i.v. infusion of (i) GLP-1 at 0.3 pmol.kg-1•min-1 (GLP-1 0.3), (ii) GLP-1 at 0.9 pmol.kg-1•min-1 (GLP-1 0.9) and (iii) 0.9% saline.
Results: GLP-1 0.3 and 0.9 slowed GE of solid (intragastric retention at t=100 min, saline: 28 ± 5%, GLP-1 0.3: 53 ± 6%, GLP-1 0.9: 58 ± 7%, P < 0.001), and liquid (T50, saline: 28 ± 2 min, GLP-1 0.3: 42 ± 7 min, GLP-1 0.9: 50 ± 9 min, P < 0.001). Both doses of GLP-1 induced "gastroparesis" in about half the cohort, and increased meal retention in the distal stomach (P < 0.05). GLP-1 attenuated the rises in glucose, insulin and GIP (P < 0.05). There was an inverse relationship between blood glucose at t=15 min and the liquid T50 (r0.70, P < 0.001).
Conclusions: In healthy subjects: (i) exogenous GLP-1 increases meal retention in the distal stomach and, even when administered in a "low" dose, frequently induces "gastroparesis" and (ii) the effects of GLP-1 on postprandial glycemia are predictable on the basis of its effect on GE, supporting the concept that GE is a major target mechanism for the clinical use of incretin mimetics.
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